Neutrophils transmigrate from the blood into inflamed tissue via the interaction of interleukin 8 (CXCL8), produced in this tissue, with chemokine receptors, CXCR1 and CXCR2 that are expressed on the membranes of neutrophils. We investigated neutrophil migration and components of this pathway in patients with inflammatory bowel disease (IBD) and healthy controls. CXCL-8 induced chemotaxis of peripheral blood isolated neutrophils was studied in a transwell system. CXCL8, CXCR1 and CXCR2 expression and CXCL8 release were examined by qRT-PCR, ELISA and immunofluorescence in neutrophils and in intestinal tissue. IBD neutrophils (n=24) show a similar chemotactic index in response to CXCL8 when compared with healthy control neutrophils (n=6), although the basal migratory capacity is a 5-fold higher. The expression of both CXCR1 and CXCR2 is increased in IBD neutrophils, while the expression and release of CXCL8 is decreased. CXCL8 protein levels were lower in non-inflamed IBD tissue homogenates (n=38) and significantly increased in inflamed IBD tissue (n=50) when compared with healthy tissue homogenates of colorectal cancer patients (n=20). CXCL8 was mainly found in epithelial cells in inflamed IBD tissue while sporadically neutrophils expressing CXCL8 were found in IBD tissue. IBD neutrophils have different expression levels of components involved in CXCL8-CXCR1/2 chemotaxis. In addition to the enhanced CXCL8 levels observed in inflamed IBD tissue, this might explain the enhanced migratory capacity of neutrophils in IBD.